Inhibitor(s) of prostaglandin biosynthesis induced by epidermal damage and detected by an oxygen consumption assay are being correlated with degrees of damage determined histologically and changes in tissue prostaglandin F2 alpha levels. Incubation studies in progress using prostaglandin dioxygenase, arachidonic acid and aliquots of homogenate from tissues with and without detectable inhibitor(s) of prostaglandin biosynthesis in the oxygen consumption assay indicate that decreased synthesis of product occurs in the presence of homogenate containing inhibitor(s). These studies will be pursued and completed. The source of increased prostaglandin F2 alpha levels in evolving patch test reactions is being investigated. Macrophages are cells that arrive late in an evolving patch test reaction in skin. The late rise in tissue prostaglandin F2 alpha noted in evolving patch test reactions may be due to synthesis by these cells. Therefore, prostaglandin biosynthesis in activated macrophages is being compared to that in control macrophages by incubations with radioactive arachidonic acid and isolation of prostaglandins E2 and F2 alpha. In addition, the activity of the enzyme, prostaglandin E2 9-ketoreductase, is being measured in these cells. Increased activity of this enzyme might convert the inflammatory mediator, prostaglandin E2, into the vasoconstrictor (in skin), prostaglandin F2 alpha. BIBLIOGRAPHIC REFERENCES: Penneys, N.S., McCreary, S., Gottlieb, N.L. The intracellular distribution of radiogold: Localization in lysosomal membranes. Arthritis and Rheumatism. 19:927-932, 1976. Penneys, N.S., Eaglestein, W.H., and Frost, R. Management of pemphigus with gold compounds. Arch. Dermatol. 112: 185-187, 1976.